Disruptions in accurate DNA replication and segregation during the cell cycle results in genomic instability and missegregation of chromosomes. Genomic instability has long been recognized as an important step in converting normal cells into neoplastic cells. Recently, an abnormal chromosomal phenotype has been described whereby there is a delay in the replication timing (DRT) of an entire chromosome. Chromosomes with DRT have been shown to be unstable and contribute to genomic instability. DRT chromosomes show a delay in the mitosis-specific phosphorylation of histone H-3 on serine 10 and a delay in mitotic chromosome condensation (DMC). H-3 phosphorylation has been shown to be an important step in chromosome condensation and segregation. Aurora B kinase is thought to be responsible for the phosphorylation of H-3. Recent results from the Thayer lab have shown that DRT chromosomes activate the replication checkpoint pathway via ATR. Therefore, I hypothesize that inhibition of Aurora B, either by inhibition of kinase activity or inhibition of recruitment to the chromosome, plays a direct role in the DMC phenotype. The objective is to characterize the link between DRT/DMC, the replication checkpoint, and Aurora B kinase. [unreadable] [unreadable]